Renal 2 Flashcards
MCC of painless hematuria (evaluation)
bladder cancer
if older than 35 –> CT and cytoscopy
gross hematuria - prostate?
BPH
not cancer
hematuria - best initial test
urinalysis to rule out and confirm microhematuria (more than 3 RBCs)
reccomendations for patient with renal calculi
- increased fluids
- low sodium
- normal calcium
medication that cause urinary retention (and manegment)
anticholinergics
stop them + cathetirization
osmolar gap?
measured serum osm - calculated serum osm
causes of combination of osmolar gap and and high anion gap met acidosis
acute ethanol (MC)
methanol
ethylen glycol
methanol toxicity
blindness
oliguria means
less than 250 ml in 12 hours
management of acute oliguria
bedside bladder scan to assess for urinary retention
- retention (MORE THAN 300 ml) –> catheter to decompress –> serum + urine bioch +/- image –> treat underling
- no retention –> serum + urine bioch +/- image:
a. pre-renal (IV fluids or treat underling)
b. renal cause -> treat underling
hepaternal vs pre-renal
hepatorenal does not respond to fluids
hepatorenal syndrome treatment
- address precipitating factor
- splachninc vasoconstrictor
- liver transplantation
MCC of death in dyalisis patients
Cardiovascular
MCC of death in patients with renal transplantation
cardiovascular
MC extrarenal manifestation of ADPKD
hepatic cysts
GI complication of ADPKD
colonic diverticula
aspirin intoxitation - ph
normal
GI symptoms of ureteral colic
vagal reaction –> ileus
medication to fascilate stone passage
a1 blocker (tamsulosin) –> act on distal ureter
bladder cancer screening
not recommended (even if RFs)
management of ureteral stones
symptomatic relief –> urosepsis, acute renal failure or complete obstructiion?
yes –> urology consult
no –> stone siize:
less than 10 mm –> hydration pain control, a blocker
bigger than 10 –> urology consult
uncontrolled pain or no stone passage in 4-6 weeks –> urology consult
MC nephrotic syndrome associated with thromboembolism
membranous nephropathy
lithium - hemodialysis?
if more than 4, or more than 2.5 with signs of toxicities
simple vs malignant renal cyst in contrast CT
only malignant has enhancement
causes of asterixis
- Hepatic encephalopathy
- Uremic encephalopathy
- CO2 retention
SIADH - management
fluid restriction +/- salt tablets
if severe: hypertonic (3%) saline
if refractory –> demeclocycline
GI loses - K+
both vomiting and diarrhea causes hypokelamia
medications that can cause hyperkalemia
- β-blockers
- ACEi
- K+ sparing diuretics
- digitalis
- cyclosporin
- heparin
- NSAID
- succinylcholine
9 . Trimethorpime
NSAID mediated hyperkalemia - mechanism
decreases renal perfusion –> decreased K delivery to the collecting ducts
Heparin mediated hyperkalemia - mechanism
blocks aldosterone production
Cyclosporine mediated hyperkalemia - mechanism
blocks aldosterone activity
Trimethoprime mediated hyperkalemia - mechanism
blockage of epithelium Na2+ channel in the collecting ducts –> also blocks the creatinine secretion (artificially), without affecting the GFR
causes of edema in nephritis
FLUID RETENTION
urinary retention due to anticholinergics
detrusor hypocotractility
medications that causes SIADH
SSRI, carbamazepine, Cyclophosphamide, NSAID
psychiatric disorder associated with 1ry polydipsia
schizophrenia
nephrotic syndrome can cause accelerated atherosclerosis - mechanism
- loss of anthothrombin III
- due to low albumin, liver overproduce lipid proteins
affects veins more (esp renal veins)
severe hyperkalemia - best initial step
calcium gluconate –> then insulin, glucose, HCO3-, β-agonists
hyperkalemia - ECG
- tall peaked T waves with short QT
- PR prolongation + QRS widening
- No P waves
- conduction block, ectopy, or sine wave pattern
metabolic acidodis - give HCO3-?
if ph less than 7.1
hypokalemia in alcohoics is refractory - why
hypogmagnesemia (removal of inhibition of renal excretion)
stones - best initial test
U/S (NOT URINALYSIS)
best options for renal transplantation
in order
- living related donor
- living unrelated
- cadaveric
drug induced intestitial nephritis - treatment
stop the related drug (not steroids)
glomerular vs non glomerulal hematuria regarding type
- glomerular usually microscopic, also proteins and casts adn dysmorphic RBCs
- nonglomerular usually gross
SE of acyclovir on kidneys (treatment)
crystaluria –> renal tubular obstruction
administer fluids with the drug
etiology of crystal induced acute kidney injury
acyclovir sulfonamides MTX ethylene glycol protease inh Uric acid
clinical presentation of crystal induced acute kidney injury
usually asymptomatic
AKI in less than 7 days from the starting drug
hematuria, pyuria, crystals
treatment of crystal induced induced acute kidney injury
stop medication
fluids
loop duretics
urinalysis - blood?
cannot distinguish Hb from myoglobin
post-void redidual volume in obstruction
more than 50 ml in men and 150 in women
renal transplantation - treatment if signs of rejection
IV steroids
renal transplant dysfunction - causes
- utreteral obstruction (U/S to rule out)
- cyclosporine toxicity (drug level)
- vascular obstruction (renal biopsy)
- acute tubular necrosis
acute rejection is treated with IV steroids
treatment of hypernatriemia
hypovolemic: O.9% saline (but if mild can give 5% dextrose in 0.45 saline)
euvolemic: hypotonic
correction no more than 1 meq/L/h
MCC of renal artery stenosis
HTN
cocaine - acute renal failure?
due to rhabdomyolisis (CPK causes ARF if more than 20.000)
the quickest way to low the K+
insulin
evaluation of met alkalosis
urine chloride
low –> vomiting / NG aspiration, prior diuretics (SALINE RESPONSIVE)
high –> hypervolemia (aldosterone) (SALINE UNRESPONSIVE)
hypovolemia/evolemia: current diuretics (SALINE RESPONSIVE) Barrter, gitelman (SALINE UNRESPONSIVE)
Most sensitive screen for nephropathy
RANDOM urine for microalbumin/creatinine ratio
24h is more accurate but it is inconvenience
advantages of renal transplantation over dyalysis
- better survival + quality
- autonomic neuropathy stabilzes or improves in diabetics
- return to normal endocrine, sexual and reproductive functions
- anemia, bone disease and hypertension better control
evaluation of hyponatremia
serum osm more than 290?
yes –> marked hypogl / advanced renal failure
no –> urine osm less than 100?:
- yes (polydipsia, malnutriotion)
- no –> check urine sodium
if if less than 25 –> SIADH, adrenal ins, hypoth
if it is more than 25 –> vloume depltion, cirrhosis, CHF
how to correct low Na+
3% salide solution
not exceed 0.5 mEg/L/hr to
characteristic of varicoceles due to underlying mass pathology
unilateral varicoceles that fail to empty when a patient s recumbent
mechanism of hepatorenal syndrome
splanchnic arterial dilation, decreaesd vascular resistance, local renal vasocnstriction with decreased perfusion
postictal lactic acidosis
anion gap metab acidosis following a tonic clonic seizure –> resolves in 90 mins without treatment
post-streptoc vs IgA nephropathy regarding complement
low C3 in post-strept
normal in IgA
reduce Ca intake - stones
reduce ca intake increases oxalate absorption
GFR in DM
increases in the beginning (hyperfiltration)
then goes down
recommendations for blood tranfusion
under 7: always
7-8: if cardiac surgery, HF, oncology patients in treatment
8-10: symptomatic anemia, noncardiac surgery, ongoing bleeding, ACS
indications for urgent dialysis
- refractory acidosis with ph under 7.1
- volume overload refractory to diuretics
- symptomatic uremia (bleeding, encephalopathy, pericarditis
- ingestion: toxic alcohols, salicylate, lithium, sodium valproate, carbamazepine
- elect abnormalities: severe or symptomatic hyperkalemia refractory to medications
skin in cyanide toxicity
cherry red flashing, cyanosis comes later
treatment of hypertension and renal artery stenosis
ACI are indicated for iniitlay therapy
renal artery stenting or surgical revasculization is resewed for patients with resistant HTN or recurrent flash pulm endam and/or refractory HF due to severe hypertension
BE VERY CAREFUL IF BILATERAL
MCC of abnormal hemostasis in patients with chronic renal failure / characteristics / treatment
platelet dysfunction
BT in elevated. PT and PTT are normal
desmoprasin is the treatment
(no transfusion)
nephrotic syndrome - anemia?
iron resistant microcytic hypochromic anemia
DUE TO TRANSFERRIN LOSS
Most frequent vessel manifestation of nephrotic syndrome
venous thrombosis
asymptomatic or mild hypercalcemia
no immediate treatment required
avoid thiazide, lithium, volume depletion + prolonged bed rest
moderate hypercalcemia - treatment
usually no immediate treatment required unless symptomatic
- similar to severe
severe hypercalcemia - treatment
short term (immediate) treatment - normal saline + calcitonin - avoid loop diuretics unless volume overload Long term - bisphosphonate
pyelonephritis treatment
- outpatient: fluoroquinolones
- inpatient: IV antibiotics (fluoroquinolone, aminoglycoside +/- ampicillin)
- urine culture prior to treatment
uncomplicated cystitis - treatment
- Nitrofurantoin for 5 fays (avoid if pyelonephritis or Cr clearance less than 60)
- TMP - sxm for 3 days
- fosfomycin (single dose)
- fluoroquinolones (2nd option)
- Culture only if initial treatment fails
complicated cystitis - treatment
- fluoroquinolones (5-14d),
- extended spectrum antibiotics (ampicillin/gentamycin) for for severe
- culture before
when is complicated cystitis
DM, kidney disease, pregnancy immunocompromised, urinary tract obstruction, hopsital acquired, assoiacetd with procedure, indwelling foreign body
treatment of uric acid stones
- hydration
- alkalinization of urine (POTASSIUM CITRATE)
- low-purine
diet - allopurinol if resistant
how to alkalinize urine in uric acid stones
potassium citrate
grades of hypercalcemia - grade
severe (more than 14) or symptomatic)
moderate: 12-14
mild or asymptomatic (less than 12)
amiloride mediated hyperkalemia - next step
change the medication
low diet K+ does not change anything
analgesic nephroapathy
MC form of drug induced chronic renal failure
Papillay necrosis + chronic tubulointestitial nephritis are the MC pathologies seen
bladder outlet obstruction (eg. from BPH) - next step
renal U/S to assess function and check for hydronephrosis
Interstitial cystisis (bladder pain syndrome) - epidimiology
- More common in women
- associaed with psychiatric + pain disorders (eg. fibromyalgia)
interstitial cystitis (bladder pain syndrome) - clinical presentation
- bladder pain with filling, releif with voiding
- urinary frequency + urgency
- Dyspareunia
interstitial cystitis (bladder pain syndrome) - diagnosis
- bladder pain with no other cause for 6 or more weeks
- normal urinalysis
interstitial cystitis (bladder pain syndrome) - treatment
- not curative: focus to improve quality of lide
- behavioral modification, avoid triggers, physical therapy
- TCA, pentosan polysulfate sodium
- Analgesics for acute exacerbations
which 2 lab values provide the best picture for acid-base status
pH + pCO2
HCO3- can be calculated fro henderson hesselbach equation
acute kidney injury causes acidosis - anion or non anion gap
both:
anion gap: uremic toxins
non-anion gap: impaired acid excretion
Obstructive uropathy - presentation
- flank pain
- low-volume voids iwth or without occasonal high-volume voids
- if bilateral: renal dysfunction
Genitourinary manifestations of diabetic autonomic neuropathy
- erectile dysfunction + retrogratde ejaculation in men, decreased libio + dyspareunia in owmen
- decreased ability to sense full bladder leading to incomplete emptying + decreased urination
- eventu`al reccurent UTI and /or overflow incontinence (dribbling, porr urinary streem
urate stones shape
needle
how to evaluate uric acid stones
CT or U/S or IV pyelography
hyperakalemia - acute therapy if
- more than 7
- ECG changes
- rapid rising
renal stones - high volume urination?
intermittent episodes of high volume urination can occur when obstruction is overcome by a large volume of reatained urine (post-obstructive) –> can lead to potassium wasting and dehydration –> weakness
postoperative oliguria with inconclusive scan - next step
folley
postoperative oliguria means
less than 0.5ml/kg/hr
suspect renal ca - next step
CT
IGA nephropathy - when is the resp infection
concurrent
aspirin ph - process
resp alkalosis early –> metabolic acidosis later